Servant Marc J, Tenoever Benjamin, Lin Rongtuan
Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical Research, and Departments of Medicine, McGill University, Montreal, Canada.
J Interferon Cytokine Res. 2002 Jan;22(1):49-58. doi: 10.1089/107999002753452656.
Recent molecular, biochemical, and gene disruption studies have demonstrated the essential role of interferon (IFN) regulatory factor-3, (IRF-3) and IRF-7 in the activation of type I IFN gene expression and the induction of the antiviral state. Both transcription factors share structural and functional properties, as well as a common mechanism of activation through C-terminal phosphorylation. The purpose of this review is to summarize recent investigations indicating that similar signalling pathways are likely involved in the activation of IRF-3 and IRF-7. Moreover, unique biochemical events, such as coactivator association and differential recognition of cis-acting elements, also illustrate the capacity of IRF-3 and IRF-7 to selectively regulate type I IFN and IFN-stimulated gene (ISG) expression.
最近的分子、生化和基因敲除研究表明,干扰素(IFN)调节因子-3(IRF-3)和IRF-7在I型IFN基因表达激活及抗病毒状态诱导中起关键作用。这两种转录因子具有结构和功能特性,以及通过C端磷酸化激活的共同机制。本综述的目的是总结近期研究,这些研究表明IRF-3和IRF-7的激活可能涉及相似的信号通路。此外,独特的生化事件,如共激活因子结合和顺式作用元件的差异识别,也说明了IRF-3和IRF-7选择性调节I型IFN和IFN刺激基因(ISG)表达的能力。